We propose a 39-week clinical study in healthy, normotensive, overweight (BMI equal to or more than 25 kg/m[2]) African American men and women aged 45 years and older that, after an initial screening and eligibility period (4 weeks), will be conducted in three phases. Phase 1 (9 weeks) begins the isocaloric 100 mmol dietary sodium diet phase. After the initial 3 weeks, a six-week period of 100 mmol/d sodium supplementation will be administered to determine salt sensitivity. Phase 2 (8 weeks) will maintain the 100 mmol sodium dietary intake and will additionally add a weight loss component to attain weight loss of about 1.5 - 2 pounds/week. Phase 3 (18 weeks) will consist of a two-period crossover trial consisting of randomization to the treatment sequence of dietary sodium supplementation of 100 mmol/d (6 weeks) followed by placebo (6 weeks) or vice versa. A 6-week placebo washout period will separate the two active periods. The 100 mmol sodium/weight loss diet from phase 2 will be maintained during this treatment phase. The difference in BP between the end of the sodium and placebo periods will determine salt sensitivty after weight loss. The overarching study hypothesis is that obesity-related salt sensitivity is attributable, in large degree, to oxidative-stress mediated reductions in nitric oxide [NO] availability. The destruction of NO is linked to obesity-related elevations of non-esterified fatty acids, leptin, and renin-angiotensin-aldosterone system activity - all of which are known to increase oxidative stress. Genetic variation in the angiotensin converting enzyme, specifically homozygosity for the insertion [I] polymorphism, will predict higher levels of salt sensitivity, oxidative stress, and lesser NO production. Environmental stressors interact with obesity to augment salt sensitivity. We further hypothesize that the degree of reversibility of salt sensitivity will closely parallel weight loss-induced reductions in oxidative stress. The primary specific aim of the study is to determine the main and interactive effects of stressors, obesity, and genetic variation of the ACE and endothelial nitric oxide synthase (eNOS) genotypes on oxidative stress and salt sensitivity and, after weight loss, to re-examine these effects as well as to link changes in oxidative stress to persistence of salt sensitivity between study phases 2 and 3. This study will provide important new insights into the pathophysiology of salt sensitivity in African Americans who are at high risk for development of hypertension and related cardiovascular diseases.